Several studies point to elevated pools of adenosine or deoxyadenosine and their metabolites as causal factors in the immunodeficiency of children with severe combined immunodeficiency disease associated with the absence of adenosine deaminase. Although measurements of purine levels and purine metabolism have not led to a unifying hypothesis for the exact biochemical mechanism by which immune function is impaired, some new features of purine metabolism in humans have been noted. Specifically, the mammalian kidney appears to have an active secretory mechanism for eliminating deoxyadenosine. We propose to characterize the system, particularly with respect to the classical active secretory systems for weak acids and strong bases.